zeaxanthin and Obesity

Age-related macular degeneration (AMD) is a major cause of visual impairment in the United States. Currently there is no effective cure for this disease. Risk factors include decreased lutein and zeaxanthin status and obesity. Obesity is also an increasing public health concern. The alarming increase in the prevalence of obesity further exacerbates the public health concern of AMD. The mechanism by which obesity increases the risk of AMD may be related to the physiologic changes that occur with this condition. These include increased oxidative stress, changes in the lipoprotein profile, and increased inflammation. These changes would also result in an increased destruction and a decreased circulatory delivery of lutein and zeaxanthin to the macula of the eye. Therefore, the mechanism by which obesity is related to AMD risk may be through indirect effects on changes in lutein and zeaxanthin status and metabolism.

Topics: Age Factors; Humans; Lutein; Macular Degeneration; Obesity; Odds Ratio; Oxidative Stress; Risk Assessment; Risk Factors; United States; Xanthophylls; Zeaxanthins

Non-alcoholic fatty liver disease (NAFLD) is a common liver disorder worldwide and a risk factor for obesity and diabetes. Emerging evidence has shown that ferroptosis is involved in the progression of NAFLD. Zeaxanthin (ZEA) is a carotenoid found in human serum. It has been reported that ZEA can ameliorate obesity, prevent age-related macular degeneration, and protect against non-alcoholic steatohepatitis. However, no study has focused on the protective effects of ZEA against NAFLD. In this study, free fatty acid (FFA) induced HepG2 cells were used as a cell model for NAFLD. Our results suggest that ZEA exerts antioxidative and anti-inflammatory effects in FFA-induced HepG2 cells. Moreover, ZEA acted as a ferroptosis inhibitor, significantly reducing reactive oxygen species (ROS) generation and iron overload and improving mitochondrial dysfunction in FFA-induced HepG2 cells. In addition, ZEA downregulated the expression of p53 and modulated downstream targets, such as GPX4, SLC7A11, SAT1, and ALOX15, which contributed to the reduction in cellular lipid peroxidation. Our findings suggest that ZEA has the potential for NAFLD intervention.

Topics: Fatty Acids, Nonesterified; Ferroptosis; Hep G2 Cells; Humans; Lipid Metabolism; Mitochondria; Non-alcoholic Fatty Liver Disease; Obesity; Tumor Suppressor Protein p53; Zeaxanthins

Cytoplasmic lipid droplets (LDs), which are remarkably dynamic, neutral lipid storage organelles, play fundamental roles in lipid metabolism and energy homeostasis. Both the dynamic remodeling of LDs and LD-mitochondrion interactions in adipocytes are effective mechanisms to ameliorate obesity and related comorbidities. Zeaxanthin (ZEA) is a natural carotenoid and has beneficial effects on anti-obesity. However, the underlying mechanisms of ZEA on LD modulation are still unclear. In the present study, ZEA efficiently inhibited LD accumulation and attenuated adipocyte proliferation by arresting the cell cycle. ZEA drove transcriptional alterations to reprogram a lipid oxidative metabolism phenotype in mature 3T3-L1 adipocytes. ZEA significantly decreased the TAG and FA content and modulated the dynamic alterations of LDs by upregulating the expression of lipases and the LD-mitochondrion contact site protein, perilipin 5 (PLIN5), and downregulating the LD fusion protein, fat-specific protein 27 (FSP27). Mechanistically, ZEA stimulated LD remodeling and ameliorated mitochondrial defects caused by large and unilocular LD accumulation by activating β3-adrenergic receptor (β3-AR) signaling. Furthermore, the knockdown of PLIN5 impaired the LD-mitochondrion interactions, thereby disrupting the role of ZEA in promoting mitochondrial fatty acid oxidation and respiratory chain operation. Collectively, the present study demonstrates that ZEA induces LD structural and metabolic remodeling by activating β3-AR signaling and enhances PLIN5-mediated LD-mitochondrion interactions in hypertrophic white adipocytes, thereby enhancing oxidative capacity, and has the potential as a nutritional intervention for the prevention and treatment of obesity and associated metabolic syndrome.

Topics: Adipocytes; Humans; Lipid Droplets; Lipid Metabolism; Lipids; Mitochondria; Obesity; Perilipin-2; Perilipin-5; Receptors, Adrenergic; Receptors, Adrenergic, beta-3; Zeaxanthins

Obesity is a worldwide epidemic associated with many health problems. One of the new trends in health care is the emphasis on regular exercise and a healthy diet. Zeaxanthin (Zea) is a carotenoid with many beneficial effects on human health. The aim of this study was to investigate whether the combination of Zea and exercise had therapeutic effects on obesity induced by an HFD in rats. Sixty male Wistar rats were randomly divided into five groups of twelve: rats fed a standard diet; rats fed a high-fat diet (HFD); rats fed an HFD with Zea; rats fed an HFD with Exc; and rats fed an HFD with both Zea and Exc. To induce obesity, rats were fed an HFD for twelve weeks. Then, Zea and exercise were introduced with the HFD for five weeks. The results showed that the HFD significantly increased visceral adipose tissue, oxidative stress, and inflammation biomarkers and reduced insulin, high-density lipoprotein, and antioxidant parameters. Treatments with Zea, Exc, and Zea plus Exc reduced body weight gain, triacylglycerol, glucose, total cholesterol, and nitric oxide levels and significantly increased catalase and insulin compared with the HFD group. This study demonstrated that Zea administration and Exc performance appeared to effectively alleviate the metabolic alterations induced by an HFD. Furthermore, Zea and Exc together had a better effect than either intervention alone.

Topics: Animals; Diet, High-Fat; Humans; Insulin; Male; Obesity; Rats; Rats, Wistar; Zeaxanthins

The xanthophyll carotenoids lutein+zeaxanthin and the dietary component choline have been linked to benefits in cognition. However, knowledge on the interactive influence of these dietary components on cognitive function is sparse.. 80 middle-aged adults with overweight and obesity (Body Mass Index: (BMI) ≥25.0 kg/m²), completed 7-day diet records, venous blood draws, heterochromatic flicker photometry, assessment of intelligence quotient (IQ), and a cognitive flexibility task while undergoing electroencephalographic recording for event-related potential (ERP) extraction. Multiplicative interaction terms and hierarchical linear regressions, controlling for age, BMI, sex, annual household income, and IQ were utilized to assess independent and interactive contributions of dietary and biomarker data on Switch task outcomes.. Higher intake of lutein+zeaxanthin and choline was associated interactively, but not independently, with faster reaction time (RT), after controlling for pertinent covariates. Dietary intake of lutein+zeaxanthin and choline was associated with serum lutein concentrations, but not with plasma choline metabolites nor macular pigmentation. Plasma phosphatidylcholine (PC) concentrations were associated with higher accuracy in Switch trials, while no other biomarkers were associated with cognitive outcomes. Dietary intake and biomarker data were not related to the N2 nor P3 ERP component.. Among a sample of adults with overweight and obesity, greater intake of choline and lutein+zeaxanthin was associated with faster performance on a cognitive flexibility task. Future work examining methods of increasing consumption of both of these dietary components as a possible means of improving or maintaining cognitive flexibility among adults with overweight and obesity is therefore warranted.

Topics: Adult; Biomarkers; Choline; Cognition; Diet; Humans; Lutein; Middle Aged; Obesity; Overweight; Zeaxanthins

The stimulation of fat thermogenesis and modulation of the gut microbiota are promising therapeutic strategies against obesity. Zeaxanthin (ZEA), a carotenoid plant pigment, has been shown to prevent various diseases; however, the therapeutic mechanism for obesity remains unclear. Herein, whether ZEA improves obesity by activating the β3-adrenergic receptor (β3-AR) to stimulate white adipose tissue (WAT) thermogenesis and modulating the gut microbiota was investigated. C57BL6/N mice were fed a high-fat diet (HFD) supplemented with ZEA for 22 weeks. ZEA treatment reduced body weight, fat weight, adipocyte hypertrophy, liver weight, and lipid deposition, and improved dyslipidaemia, serum GPT, GOT, leptin, and irisin levels, glucose intolerance, and insulin resistance in HFD-fed mice. Mechanistically, ZEA treatment induced the expression of β3-AR and thermogenic factors, such as PRDM16, PGC-1α, and UCP1, in inguinal WAT (iWAT) and brown adipose tissue. ZEA treatment stimulated iWAT thermogenesis through the synergistic cooperation of key organelles, which manifested as an increased expression of lipid droplet degradation factors (ATGL, CGI-58 and pHSL), mitochondrial biogenesis factors (

Topics: Adipose Tissue; Animals; Disease Models, Animal; Energy Metabolism; Gastrointestinal Microbiome; Male; Mice; Mice, Inbred C57BL; Obesity; Receptors, Adrenergic; Signal Transduction; Thermogenesis; Zeaxanthins

Obesity is closely associated with maintaining mitochondrial homeostasis, and mitochondrial dysfunction can lead to systemic lipid metabolism disorders. Zeaxanthin (ZEA) is a kind of carotenoid with potent antioxidant activity and has been reported to promote mitochondrial biogenesis. Nevertheless, the molecular mechanism has not been explained. In this study, we first discovered that ZEA stimulated 3T3-L1 adipocyte browning by increasing the expression of specific markers (Cd137, Tbx1, Sirt1, Cidea, Ucp1, Tmem26, and Cited1), thereby reducing lipid accumulation. Besides, ZEA promoted mitochondrial biogenesis by increasing the expression of PRDM16, UCP1, NRF2, PGC-1α, and SIRT1. Moreover, the uncoupled oxygen consumption rate (OCR) of protons leaked in 3T3-L1 adipocytes was rapidly increased by ZEA treatment, which improved mitochondrial respiration and energy metabolism. Furthermore, we found that ZEA promotes browning by enhancing mitochondrial biogenesis partly through the protein kinase A (PKA) pathway. This study provided new insight into the promotion of browning and mitochondrial biogenesis by ZEA, suggesting that ZEA probably has potential therapeutic effects on obesity.

Topics: 3T3-L1 Cells; Adipocytes, Brown; Animals; Antioxidants; Cyclic AMP-Dependent Protein Kinases; Energy Metabolism; Mice; Mitochondria; Molecular Docking Simulation; Obesity; Organelle Biogenesis; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; Sirtuin 1; Thermogenesis; Transcription Factors; Uncoupling Protein 1; Zeaxanthins

Macular accumulation of xanthophyll carotenoids (lutein, zeaxanthin) is known to have neuroprotective potential, yet their influence on cognition among overweight adults and those with obesity remains limited. This study examines the impact of macular xanthophylls on attentional resource allocation and information processing speed among adults with BMI ≥ 25 kg m. Adults between 25 and 45 years (N = 101) complete heterochromatic flicker photometry to determine macular pigment optical density (MPOD). Event-related brain potentials are recorded during a visual oddball task. Amplitude and latency of the N2 and P3 indexed attentional resource allocation and information processing speed. Covariates included age, sex, education, intelligence quotient (IQ), %Fat (DXA), and dietary lutein and zeaxanthin (Diet History Questionnaire II). MPOD is inversely related to P3 peak amplitude during standard trials and P3 peak latency during target trials. Therefore, individuals with higher MPOD dedicate fewer attentional resources when attentional demands are low while exhibiting faster information processing speed when attentional demands are increased. Further, MPOD is inversely related to the N2 mean amplitude during targets, signifying greater inhibitory control.. These findings are the first to link macular xanthophylls to neuroelectric indices of attentional and inhibitory control among adults with overweight and obesity.

Topics: Adult; Diet; Evoked Potentials; Female; Humans; Lutein; Macular Pigment; Male; Middle Aged; Obesity; Overweight; Xanthophylls; Zeaxanthins

Several studies associated high-fat intakes with a high incidence of age-related macular degeneration (AMD). Lutein and Zeaxanthin isomers (L/Zi) may counteract reactive oxygen species produced by oxidative stress. The present study was conducted to determine the possible effects of L/Zi administration on lipid profile, protein genes associated with oxidative stress and inflammation pathways in the obesity induced by a high-fat diet (HFD) in rodents.. Twenty-eight male Wistar rats were allocated into four groups as follows: (i) Control, (ii) Control + L/Zi, (iii) High Fat Diet (HFD), and (iv) HFD+ L/Z. L/Zi was administrated for 8 weeks at a daily dose of 100 mg/kg BW.. L/Zi administration significantly reduced insulin and free fatty acid (FFA) levels (P < 0.001) and ameliorated the oxidative damage by reducing malondialdehyde (MDA) concentration and increasing antioxidant enzymes activities of retina induced by HFD. In addition, supplementation decreased the levels of vascular endothelial growth factor (VEGF), inducible nitric oxide synthase (iNOS), nuclear factor-kappa B (NF-κB) and intercellular adhesion molecule-1 (ICAM) (P < 0.001, respectively) and improved nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) gene proteins in retinal tissues (P < 0.001).. Rats fed with HFD exhibited increased oxidative stress and upregulation of inflammatory indicators. However, L/Zi supplementation modulates genes involved oxidative stress and inflammation including NF-κB and Nrf2 signaling pathways in the retina which may contribute to ameliorating retinal damage induced by HFD.

Topics: Animals; Blotting, Western; Diet, High-Fat; Disease Models, Animal; Lipid Metabolism; Lutein; Male; Obesity; Oxidative Stress; Rats; Rats, Wistar; Retina; Zeaxanthins

Zeaxanthin, a type of carotenoid, has been proven to exhibit anti-lipogenesis effect; however, the detailed mechanism of this effect is less known. Herein, we evaluated the effects of zeaxanthin on the inhibition of adipogenesis in 3T3-L1 adipocytes and obesity in high-fat diet fed C57BL/6J mice. Zeaxanthin significantly decreased the intracellular lipid content in a dose-dependent manner (5-15 μM) in adipocytes without causing cytotoxicity. In high-fat-diet-induced obese mice, oral administration of 20 mg kg

Topics: 3T3-L1 Cells; Adipocytes; Adipogenesis; AMP-Activated Protein Kinase Kinases; Animals; Anti-Obesity Agents; Diet, High-Fat; Humans; Male; Mice; Mice, Inbred C57BL; Mice, Obese; Obesity; PPAR gamma; Protein Kinases; Zeaxanthins

Many epidemiological studies find an inverse correlation between carotenoids intake or carotenoids plasma concentrations and body mass index (BMI), insulin resistance or metabolic syndrome in the general population. However, it is not clear whether these relationships occur in obese population.. We conducted a cross-sectional study in 108 obese non-diabetic patients.. There was an inverse correlation between plasma levels of pro-vitamin A carotenoids (α-carotene, β-carotene and β-cryptoxanthin) and both BMI and insulin resistance (estimated by the HOMA-IR). No correlation between plasma concentrations of lycopene or lutein/zeaxanthin and BMI or insulin resistance was found. The inverse association between the three pro-vitamin A carotenoids and HOMA-IR disappeared after adjustment for BMI and waist circumference. Interestingly, we identified a positive association between concentrations of β-carotene and adiponectin in plasma that was independent of sex, age, smoking status, BMI and waist circumference. To our knowledge, such association has never been described in obese patients.. These results suggest the existence of a favourable effect of β-carotene on insulin sensitivity in obese individuals that could involve a positive regulation of adiponectin, either directly or via its pro-vitamin A activity. The demonstration of the potential benefits of β-carotene towards insulin sensitivity would open the way to dietary strategies to prevent metabolic syndrome.

Topics: Adiponectin; Adolescent; Adult; Aged; beta Carotene; Body Mass Index; Carotenoids; Cholesterol, HDL; Cholesterol, LDL; Cross-Sectional Studies; Diabetes Mellitus; Diet; Female; Humans; Insulin Resistance; Interleukin-1; Leptin; Linear Models; Lutein; Lycopene; Male; Metabolic Syndrome; Middle Aged; Multivariate Analysis; Obesity; Plasminogen Activator Inhibitor 1; Triglycerides; Tumor Necrosis Factor-alpha; Young Adult; Zeaxanthins

To assess the characteristics of patients with wet AMD and low intake of lutein and zeaxanthin in our population.. A prospective, observational, cross-sectional study was conducted on patients with active wet AMD. A full blood count, a lipid and liver profile, a dietary interview (24-hour recall), and an anthropometric study were performed. Lutein-zeaxanthin (LZ) intake results split the patents in two groups.Group 1 ("sufficient" intake): patients with ≥1,400 mg/day intake in women and 1,700 mg/day in men (2/3 of the average daily intake in a normal population). Group 2: patients with daily intakes below that of group 1. A descriptive and comparative statistical study was performed.. Fifty-two patients with a mean age of 78.9 years. Group 1: eleven patients (21% of the sample). Group 2: forty-one patients. The subjects with adequate intake of LZ had higher a body mass index and waist circumference. Between 70-80% of patients in group 1 had inadequate intake of vitamin A, C and E and zinc.. Seventy-nine per cent of the patients with wet AMD have a deficient daily intake in lutein-zeaxanthin. The population with adequate intake is associated with an increased body mass index and waist circumference, and in addition, most of them have an insufficient intake of vitamin A, C, E and zinc.

Topics: Aged; Antioxidants; Cardiovascular Diseases; Comorbidity; Cross-Sectional Studies; Diet; Diet Records; Diet, Mediterranean; Dyslipidemias; Female; Humans; Lutein; Male; Micronutrients; Obesity; Prospective Studies; Spain; Vitamins; Wet Macular Degeneration; Xanthophylls; Zeaxanthins; Zinc

Lifestyle, diet, and physical and health predictors of xanthophyll carotenoids in the retina are poorly understood.. We aimed to investigate the predictors of the density of lutein and zeaxanthin in the macula of the retina.. Macular pigment optical density (MPOD) was measured by heterochromatic flicker photometry. Relations to dietary lutein and zeaxanthin and to other predictors were measured in 1698 women aged 53-86 y. The women were members of observational study cohorts of the Women's Health Initiative at Iowa City, IA, Madison, WI, or Portland, OR, and participated in the Carotenoids in Age-Related Eye Disease Study (2001-2004).. MPOD at 0.5 degrees from the foveal center was 30% higher in women in the highest quintile for lutein and zeaxanthin intake [x (+/-SD): 0.40 +/- 0.21] than in women in the lowest quintile (0.31 +/- 0.21) and 20% higher after adjustment for other predictors. Dietary intake of lutein, zeaxanthin, fiber, and polyunsaturated fatty acids (% of energy) together explained 3% of the variability in MPOD. Higher waist circumference and diabetes, which are related to lower MPOD, together with study site explained an additional 5% of variation. The total explained variability increased to 12% when lutein and zexanthin concentrations obtained from the serum, which were collected 4-7 y earlier, were added to the model.. MPOD is directly related to dietary intake of lutein and zeaxanthin but even more strongly to serum concentrations, which may reflect unmeasured physical and medical factors that influence the uptake, distribution, and utilization of lutein and zeaxanthin. Higher abdominal body fat and diabetes are related to lower MPOD. Unknown predictors of retinal carotenoids remain.

Topics: Aged; Aged, 80 and over; Aging; Cohort Studies; Diet; Female; Humans; Lutein; Macula Lutea; Macular Degeneration; Middle Aged; Obesity; Prospective Studies; Retina; United States; Women's Health; Xanthophylls; Zeaxanthins

Because of the potential protective function of lutein (L) and zeaxanthin (Z) within the retina and lens, a better understanding of factors influencing tissue deposition is needed. The largest fractions of L and Z are stored in adipose tissue. Thus, higher body fat content and body mass index (BMI) may be expected to influence the quantities of L and Z in the retina (measured as macular pigment optical density, MPOD).. Six hundred eighty subjects were tested. Information on MPOD, body mass index (BMI), body fat percentage (n = 400, using bioelectric impedance), dietary intake (n = 280, using a food frequency questionnaire), and serum carotenoid content (n = 280, using reversed phase high-performance liquid chromatography) was obtained.. There was an inverse relationship between MPOD and BMI (n = 680, r = -0.12, P < 0.0008) and between MPOD and body fat percentage (n = 400, r = -0.12, P < 0.01). These relationships were largely driven by data from the subjects with higher BMI (more than 29, 21% less MP) and higher body fat percentage (more than 27%, 16% less MP). Dietary carotenoid intake and serum carotenoid levels were also lower in subjects with higher BMI (n = 280).. Obese subjects tend to have lower retinal L and Z. This reduction may be due to decreased dietary intake of L and Z and/or competition between retina and adipose tissue for uptake of L and Z.

Topics: Adipose Tissue; Adult; Anthropometry; beta Carotene; Body Mass Index; Carotenoids; Chromatography, High Pressure Liquid; Electric Impedance; Energy Intake; Feeding Behavior; Female; Humans; Lutein; Male; Obesity; Retina; Retinal Pigments; Xanthophylls; Zeaxanthins